Approach to the infant or child with nausea and vomiting

INTRODUCTION Nausea and vomiting are common sequelae of a multitude of disorders

that can range from mild, self-limited illnesses to severe, life-threatening conditions. Vomiting
and nausea may or may not occur together, or may be perceived at the same level of intensity. As
an example, vomiting can occur without preceding nausea in individuals with mass lesions in the
brain or increased intracranial pressure (ICP). Furthermore, some medications may alleviate
nausea but not vomiting, or vice versa.
The symptoms of nausea and vomiting may be caused by many pathologic states involving
several systems (including gastrointestinal, neurologic, renal, and psychiatric). Younger children
may not be able to describe nausea, which may further complicate diagnosis. The best course of
action should be dictated by the medical history, taking into consideration clinical features of
specific disorders and their relative frequency among children in different age groups. The most
important consideration during the initial encounter is recognition of serious conditions, such as
intestinal obstruction and increased ICP, for which immediate intervention is required. (See
'Concerning signs' below.)
This topic review will provide an overview of the neurophysiology and differential diagnosis of
nausea and vomiting in children, while suggesting a general approach to specific testing.
Individual disorders are discussed in further detail in linked topic reviews. Several
gastrointestinal disorders present with abdominal pain in addition to nausea and vomiting, and
these are discussed below. However, evaluation of the child in whom abdominal pain is the
primary presenting complaint is discussed separately. (See "Emergent evaluation of the child
with acute abdominal pain" and "Chronic abdominal pain in children and adolescents: Approach
to the evaluation".)
DEFINITIONS
Vomiting (emesis) refers to the forceful oral expulsion of gastric contents associated with
contraction of the abdominal and chest wall musculature. Vomitus often has a slight yellow tinge,
which is caused by reflux of small amounts of bile into the stomach. Vomitus is considered
bilious if it has a green or bright yellow color, indicating larger amounts of bile in the stomach;
bilious vomiting is often associated with intestinal obstruction, as described below.
Nausea generally refers to an unmistakable sensation of unpleasantness that may precede
vomiting, but may be present even in a child who does not vomit. It is often associated with
autonomic changes such as salivation, increased heart and respiratory rates, and a reduction in
gastric tone and mucosal blood flow [1]. Although there is no forceful expulsion of gastric
contents with nausea, there may be retrograde reflux of fluids from the duodenum to the gastric
antrum.
The related terms, regurgitation, anorexia, sitophobia, early satiety, retching, and rumination are
defined in the table (table 1).

PHYSIOLOGY OF EMESIS
Neurophysiology Vomiting may have a physiologic benefit since it provides a means to expel
potential toxins. Nausea and vomiting may also induce a conditioned aversion to ingested toxins
[2]. In disease states, however, vomiting pathways are activated inappropriately. The major
pathways through which nausea and vomiting are induced are vagal afferents, the area postrema,
the vestibular system, and the amygdala [1]. Five principal neurotransmitter receptors mediate
vomiting: muscarinic (M1), dopamine (D2), histamine (H1), serotonin (5-hydroxytryptamine [5HT3]), and substance P (neurokinin 1). (See "Characteristics of antiemetic drugs".)
Vagal afferent pathway Abdominal vagal afferents are involved in the emetic response.
These pathways can be evoked by either mechanical or chemosensory sensations. Examples of
sensations that trigger this pathway include overdistension, food poisoning, mucosal irritation,
cytotoxic drugs, and radiation [2]. Vagal afferents are an important site of action of 5-HT3
receptor antagonists used as antiemetic drugs [1].
Area postrema The area postrema has been referred to as the "chemoreceptor trigger zone."
Anatomically, this region is located at the caudal extremity of the floor of the fourth ventricle.
Because the area postrema represents a relatively permeable blood-brain barrier region, it is the
place where many, but not all, systemic chemicals act to induce emesis [1]. The area postrema is
an important site for M1, D2, 5-HT3, and neurokinin 1 (NK1) receptors, each of which is a key
mediator of vomiting.
Vestibular system The vestibular system is involved in the emetic response to motion. This
response is often exacerbated when vestibular input is in conflict with visual sensations [2].
Irritation or labyrinthine inflammation can produce vomiting. Others have suggested that
overstimulation of the vestibular system is not a complete explanation for motion sickness, and
that circulating neuroactive compounds may be involved. H1 receptors in the vestibular nucleus
have a role in this response.
Amygdala The amygdala is involved in a variety of stress and emotional responses. Among
other structures, it receives input from the olfactory bulb and olfactory cortex and sends impulses
to the hypothalamus. Aberrant activation of the amygdala may lead to a sensation of nausea.
Somatomotor events The act of vomiting represents a highly coordinated sequence of events.
As noted above, vomiting describes the act of emptying out the stomach, characterized by cycles
of retching followed by the forceful expulsion of gastric contents. The detailed sequence of
events is as follows [1]:
The diaphragm descends and the intercostal muscles contract while the glottis is closed.
The abdominal muscles contract and the gastric contents are forced into upper gastric vault and
lower esophagus.
The abdominal muscle relaxes and the esophageal refluxate empties back into the gastric vault.

Several cycles of retching, each more rhythmical and forceful in nature, occur, with shorter
intervals in between.
Abdominal contraction associated with elevation of diaphragms results in forceful expulsion of
gastric contents.
APPROACH TO MANAGEMENT Patients with acute vomiting, typically for hours to a few
days, most often present to an emergency department, whereas patients with chronic symptoms
are more often initially evaluated in outpatient office settings. Emergency department clinicians
should expeditiously exclude life-threatening disorders such as bowel obstruction, diabetic
ketoacidosis, adrenal crisis, toxic ingestion, or increased intracranial pressure (ICP) (table 2).
In both urgent care and routine outpatient settings, the following three steps should generally be
undertaken in patients with nausea and vomiting:
The etiology should be sought, taking into account the child's age, and whether the nausea and
vomiting is acute, chronic, or episodic.
The consequences or complications of nausea and vomiting (eg, fluid depletion, hypokalemia,
and metabolic alkalosis) should be identified and corrected.
Targeted therapy should be provided, when possible (eg, surgery for bowel obstruction or
dietary changes for food sensitivity). In other cases, the symptoms should be treated.
EVALUATION A careful history and physical examination should be performed. In many
cases, the cause of the nausea and vomiting can be determined from the history, and physical
examination and additional testing is not required. The urgency with which various diagnostic
possibilities should be pursued depends upon a number of factors, including the duration of
illness, overall clinical status of the patient (especially hydration, circulatory, and neurologic
status), and associated findings.
Concerning signs Warning signs that may indicate a serious cause of vomiting include (table
3):
Nonspecific symptoms
Prolonged vomiting
Profound lethargy
Significant weight loss
Symptoms of gastrointestinal obstruction or disease
Bilious vomiting

Projectile vomiting in an infant three to six weeks of age

Hematemesis
Hematochezia (rectal bleeding)
Marked abdominal distension and tenderness
Symptoms or signs suggesting neurologic or systemic disease
Bulging fontanelle in a neonate or young infant
Headache, positional triggers for vomiting or vomiting on awakening, and/or lack of nausea
Altered consciousness, seizures, or focal neurologic abnormalities
History of head trauma
Hypotension disproportionate to the apparent illness, and/or hyponatremia and hyperkalemia
Patients should be referred to a pediatric gastroenterologist or other appropriate specialist (eg,
pediatric surgeon, neurologist) when there are symptoms or physical findings that are of
particular concern. Immediate pediatric surgical consultation is warranted if appendicitis, bowel
obstruction, or bowel perforation are suspected.
History The history should detail the onset and pattern of the vomiting or nausea (acute,
chronic, or episodic), and associated symptoms, especially fever, abdominal pain, diarrhea, or
headache (table 4). Recent exposures to contacts with similar symptoms should be explored, as
well as a history of ingestion, or opportunity for ingestion, of medications or toxic substances.
Key information from the child's past medical history includes known or suspected congenital
anomalies or diseases, developmental delay, and neurologic symptoms or disorders.
The following clinical features are especially important:
Nature of vomiting:
Bilious (green or bright yellow) vomiting suggests intestinal obstruction, especially in a neonate
(eg, due to intestinal atresia or volvulus) [3]. (See 'Intestinal obstruction' below and
'Intussusception' below.)
Projectile (very forceful) vomiting in an infant three to six weeks of age suggests pyloric
stenosis. (See 'Pyloric stenosis' below.)
Bloody vomiting (hematemesis) suggests bleeding from esophageal varices if severe.
Hematemesis also may be caused by esophageal injury from recurrent vomiting (Mallory-Weiss

tear), or mucosal injury from erosive esophagitis, gastritis, or peptic ulcer. (See "Mallory-Weiss
syndrome" and "Approach to upper gastrointestinal bleeding in children", section on 'Etiology'.)
Periodic episodes of vomiting suggest inborn errors of metabolism, especially in a newborn or
young infant, or cyclic vomiting syndrome. (See 'Inborn errors of metabolism' below and 'Cyclic
vomiting syndrome' below.)
Early morning nausea or vomiting suggests pregnancy, increased intracranial pressure (ICP), or
cyclic vomiting syndrome. (See 'Intracranial hypertension' below.)
Prolonged vomiting (eg, >12 hours in a neonate; >24 hours in children younger than two years;
>48 hours in older children) suggests a cause that may require intervention, such as obstruction,
metabolic disorder, or cyclic vomiting syndrome. In addition, patients with prolonged vomiting
are at risk for developing dehydration and electrolyte abnormalities.
Positional triggers for vomiting or vomiting on awakening, lack of associated nausea, and/or
headache suggests increased ICP. (See 'Intracranial hypertension' below.)
Associated symptoms:
Diarrhea (with or without fever) in a patient with acute onset of vomiting is consistent with viral
gastroenteritis. This possibility is supported by a history of close contacts with vomiting and/or
diarrhea and suggests gastroenteritis. However, more serious causes of these symptoms should
be considered in patients with atypical features. These causes include infection (sepsis, infectious
enteritis/colitis, appendicitis, or inflammatory bowel disease [IBD]), and Hirschsprung diseaseassociated enterocolitis (especially in neonates or infants with risk factors, such as trisomy 21).
(See 'Gastroenteritis' below.)
Rectal bleeding (hematochezia) suggests intussusception (especially in infants and toddlers),
infectious colitis, or IBD. (See 'Intussusception' below and 'Inflammatory bowel disease' below.)
Fever is associated with many causes of nausea and vomiting, including viral gastroenteritis,
appendicitis, streptococcal pharyngitis, urinary tract infection, and sometimes IBD. (See
'Gastroenteritis' below and 'Appendicitis' below and 'Other infections' below and 'Inflammatory
bowel disease' below.)
A history of chronic or recurrent infections raises the possibility of an immunodeficiency.
Recurrent pneumonia in an infant also may be caused by a tracheoesophageal fistula. (See
"Approach to the child with recurrent infections" and "Congenital anomalies of the intrathoracic
airways and tracheoesophageal fistula", section on 'Tracheoesophageal fistula and esophageal
atresia'.)
Prominent headache associated with nausea can be consistent with either migraine or increased
ICP. (See 'Migraine' below and 'Intracranial hypertension' below.)

Physical examination The physical examination should include a detailed evaluation of the
abdomen for signs of obstruction or focal tenderness, as well as a neurologic assessment (table
4).
Abdominal examination:
Signs suggestive of intestinal obstruction include marked abdominal distension; visible bowel
loops; absent bowel sounds or increased high-pitched bowel sounds ("borborygmi"); severe
abdominal pain; or vomitus that is bilious (green or yellow) or feculent (with the odor of feces).
By contrast, milder abdominal distension and active bowel sounds with normal pitch are
common in simple gastroenteritis. (See 'Intestinal obstruction' below and 'Intussusception'
below.)
Focal abdominal tenderness in the right lower quadrant suggests appendicitis or Crohn disease.
Focal tenderness in the right upper quadrant suggests gallbladder disease (cholelithiasis or
cholecystitis) or pancreatitis. Tenderness in the costovertebral angle suggests pyelonephritis.
Abdominal pain or tenderness in the epigastric area is nonspecific, but is also consistent with
esophagitis, gastritis, peptic ulcer disease, or pancreatitis. (See 'Appendicitis' below and
'Inflammatory bowel disease' below.)
Hepatomegaly, splenomegaly, or jaundice may be caused by hepatitis, viral infection, or
metabolic disorders. (See 'Inborn errors of metabolism' below.)
Neurologic examination:
Altered consciousness, seizures, or focal neurologic abnormalities may be caused by toxic
ingestion, diabetic ketoacidosis, central nervous system mass, or inborn error of metabolism.
Bulging fontanelle in a neonate or young infant suggests the possibility of hydrocephalus or
meningitis.
Ataxia, dizziness, or nystagmus (eye twitching) suggest vestibular neuronitis or acute cerebellar
ataxia. (See "Evaluation of dizziness in children and adolescents" and "Acute cerebellar ataxia in
children".)
Other findings:
Ambiguous genitalia and/or hyperkalemia suggest the possibility of adrenal crisis (usually due
to congenital adrenal hyperplasia). (See 'Adrenal insufficiency' below.)
An unusual odor emanating from the patient should prompt an investigation for metabolic
causes of vomiting. (See 'Inborn errors of metabolism' below and "Inborn errors of metabolism:
Epidemiology, pathogenesis, and clinical features", section on 'Abnormal odors'.)
Enlarged parotid glands in an adolescent should raise suspicion for bulimia. (See 'Bulimia or
psychogenic vomiting' below.)

Laboratory testing For patients with vomiting that is severe, prolonged (eg, >12 hours in a
neonate; >24 hours in children younger than two years; >48 hours in older children) or
unexplained, screening laboratory tests should include a complete blood count, electrolytes,
glucose, blood urea nitrogen (BUN), amylase, lipase, liver aminotransferases, and urinalysis. For
patients with fever, urinary symptoms, or diarrhea, the evaluation may include urine culture and
stool studies for occult blood, leukocytes, bacterial pathogens, and parasites.
Additional laboratory testing and imaging should be tailored to the differential diagnosis of the
symptoms, based upon the history and physical examination (table 5).
DIFFERENTIAL DIAGNOSIS OF VOMITING BY AGE GROUP The differential diagnosis
of vomiting varies with the age of the child (table 2). The following sections will summarize the
clinical features of the relatively common disorders and the less common but serious disorders in
various age groups. Many of these disorders occur in several age ranges, but are discussed below
within the age group in which they present most frequently.
Neonates and young infants Uncomplicated gastroesophageal reflux, characterized by
effortless regurgitation, is common and inconsequential in otherwise healthy infants. By contrast,
forceful and repeated vomiting in infants is not normal and should be taken seriously,
particularly if there are other signs of illness (eg, fever, weight loss, or feeding refusal).
Important causes of these symptoms include pyloric stenosis and intestinal obstruction (table 6).
Other conditions that may present with vomiting are sepsis, excessive feeding volume,
hydrocephalus, or inborn errors of metabolism.
Gastroesophageal reflux disease Physiologic gastroesophageal reflux in newborns and infants
is common, and is characterized by effortless regurgitation in an otherwise healthy infant (a
"happy spitter"). This symptom may be described as vomiting by parents. The symptom
gradually improves in most infants during the first year of life, and may be minimized by
conservative antireflux measures [4]. (See "Gastroesophageal reflux in infants".)
A minority of infants who regurgitate have pathological gastroesophageal reflux, termed
gastroesophageal reflux disease (GERD). No specific clinical features definitively identify these
infants, but they may have recurrent fussiness or irritability and feeding aversion. These
symptoms are thought to result from pain caused by esophageal acid exposure. Bradycardia or
cyanotic episodes also may occur, particularly in preterm or neurologically-impaired infants.
Poor weight gain despite an adequate intake of calories should prompt evaluation for causes of
vomiting and weight loss other than GERD. (See "Gastroesophageal reflux in infants", section
on 'Management by presenting symptoms'.)
GERD also is an important consideration in older infants, children, and adolescents presenting
with subacute or chronic nausea or vomiting. The assessment and management of this disorder
are discussed in separate topic reviews. (See "Clinical manifestations and diagnosis of
gastroesophageal reflux disease in children and adolescents" and "Management of
gastroesophageal reflux disease in children and adolescents".)

Food protein-induced enteropathy Intolerance to dietary proteins (most commonly milk

protein) typically manifests as colitis, presenting with bloody stools. However, in some infants
the dietary protein causes enteritis, with or without associated colitis, and affected infants may
present with vomiting, diarrhea, and failure to thrive. In contrast to food allergy/anaphylaxis,
these disorders are not mediated by immunoglobulin E (IgE), and tend to have subacute or
delayed onset. (See "Food protein-induced proctitis/colitis and enteropathy of infancy".)
Food protein-induced enterocolitis syndrome Food protein-induced enterocolitis syndrome
(FPIES) is a gastrointestinal food hypersensitivity that manifests as profuse, repetitive vomiting,
often with diarrhea, leading to dehydration and lethargy in the acute setting, or weight loss and
failure to thrive in a chronic form. The disease usually begins in early infancy, within one to four
weeks following introduction of cow's milk or soy protein. It is most commonly caused by cow's
milk or soy protein, although other foods can be triggers; it is uncommon in breastfed infants.
FPIES is a non IgE-mediated reaction to food, similar to food protein-induced enteropathy, but
with more severe manifestations. (See "Food protein-induced enterocolitis syndrome (FPIES)".)
Pyloric stenosis Infantile hypertrophic pyloric stenosis (IHPS) is a condition of hypertrophy
of the pylorus, with elongation and thickening, eventually progressing to near-complete
obstruction of the gastric outlet. It occurs in approximately 3 in 1000 live births, more commonly
in males (4:1 to 6:1). Approximately 30 percent of cases occur in firstborn children. (See
"Infantile hypertrophic pyloric stenosis".)
The classic presentation of IHPS is the three- to six-week-old baby who develops immediate
postprandial, nonbilious, often projectile vomiting and demands to be re-fed soon afterwards (a
"hungry vomiter"). In the past, patients were classically described as being emaciated and
dehydrated with a palpable "olive-like" mass at the lateral edge of the rectus abdominus muscle
in the right upper quadrant of the abdomen. Laboratory evaluation classically showed a
hypochloremic, metabolic alkalosis resulting from the loss of large amounts of gastric
hydrochloric acid, the severity of which depended upon the duration of symptoms prior to initial
evaluation.
The typical presentation has changed over time. Infants are diagnosed earlier, tend to be better
nourished, and generally present without significant electrolyte imbalances. The diagnosis is
made by ultrasound examination of the abdomen (table 7) [5]. (See "Infantile hypertrophic
pyloric stenosis".)
Adrenal insufficiency Infants presenting with symptoms similar to those of pyloric stenosis,
but with hyponatremia, hyperkalemic acidosis, and/or disproportionate hypotension, should raise
concern for adrenal crisis. This is a life-threatening condition and should be evaluated and treated
urgently.
The most common cause of adrenal insufficiency in infants is congenital adrenal hyperplasia
(CAH) due to 21-hydroxylase deficiency. In the United States, 21-hydroxylase deficiency is part
of the newborn screen in most states, so most such infants will be diagnosed prior to developing
adrenal crisis. Adrenal crisis usually presents between the first and fourth week of life. Affected
females will have ambiguous genitalia; males usually have no obvious genital abnormalities.

(See "Causes and clinical manifestations of primary adrenal insufficiency in children", section on
'Adrenal crisis'.)
Intestinal obstruction There are multiple causes of intestinal obstruction in neonates and
young infants [6]. Causes of intestinal obstruction that present during early infancy include:
Intestinal atresia (see "Intestinal atresia")
Hirschsprung disease (see "Congenital aganglionic megacolon (Hirschsprung disease)")
Pyloric stenosis (see 'Pyloric stenosis' above)
Malrotation with or without volvulus (see "Intestinal malrotation")
Intussusception (see 'Intussusception' below and "Intussusception in children")
Bilious (bile-stained) vomitus in a neonate should be treated as a life-threatening emergency
because this is often a symptom of obstruction due to intestinal atresia or mid-gut volvulus [3],
although bilious vomiting can be seen occasionally in infants without bowel obstruction.
Vomiting that is not bile-stained may be caused by proximal obstruction, such as pyloric stenosis,
upper duodenal stenosis, gastric volvulus, or annular pancreas [7].
If intestinal obstruction is suspected, the specific diagnosis often can be suggested by the
patient's history and with appropriate radiologic imaging. Plain radiographs of the abdomen
generally provide a rapid assessment of possible bowel obstruction with relatively little radiation
exposure (table 7). Abdominal ultrasound provides high sensitivity and specificity for detecting
intussusception. If a diagnosis is not established by ultrasound and proximal bowel obstruction is
suspected, then an upper gastrointestinal contrast study usually is appropriate for. If the
abdominal radiograph or physical examination suggests distal bowel obstruction (as might be
seen in Hirschsprung disease), then a contrast enema usually is appropriate. (See
"Intussusception in children".)
Malrotation with volvulus Malrotation is an anomaly of fetal intestinal development that
occurs in about 1 in 6000 newborns. In this condition, the cecum is abnormally positioned in the
right upper quadrant, and is fixated to the right lateral abdominal wall by bands of peritoneum.
These abnormalities predispose to intestinal volvulus, in which the intestine twists on its
mesentery. This causes acute small bowel obstruction and ischemia, which usually presents with
sudden onset of bilious vomiting and an acute abdomen. Volvulus occurs early in infancy in
approximately one-half of infants with malrotation. Other infants with malrotation may remain
asymptomatic or present later in childhood with volvulus. Affected infants also may present with
signs of duodenal obstruction or with associated congenital anomalies such as intestinal atresias.
(See "Intestinal malrotation".)
Hirschsprung disease Most patients with Hirschsprung disease are diagnosed in the neonatal
period. Patients present with symptoms of distal intestinal obstruction: bilious emesis, abdominal
distension, and failure to pass stool. The diagnosis can be suggested by a delay in passage of the

first meconium (greater than 48 hours of age). Affected children may also present initially with
enterocolitis, a potentially life-threatening illness in which patients have a sepsis-like picture
with fever, vomiting, diarrhea, and abdominal distension, which can progress to toxic
megacolon. (See "Congenital aganglionic megacolon (Hirschsprung disease)".)
Inborn errors of metabolism Inborn errors of metabolism are rare causes of vomiting in
neonates and young infants. Nonetheless, recognition of these disorders is important because the
institution of appropriate therapy can be life-saving. The clinical presentation varies with the
type of metabolic disorder.
Organic acidemias and urea cycle disorders are characterized by recurrent episodes of vomiting
and dehydration (see "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical
features" and "Inborn errors of metabolism: Metabolic emergencies"):
Organic acidemias The typical presentation of organic acidemias in newborns is an acute,
severe illness characterized by lethargy, poor feeding, vomiting, metabolic acidosis, and shock.
(See "Organic acidemias".)
Urea cycle disorders Urea cycle disorders typically present during infancy or early
childhood, with episodes of altered mental status with gastrointestinal symptoms and
hyperammonemia, often triggered by catabolic stress (intercurrent illness or fasting) or increased
protein load. (See "Urea cycle disorders: Clinical features and diagnosis".)
Disorders of carbohydrate intolerance are triggered by specific sugars in the diet; non-glucose
reducing substances are usually present in the urine:
Galactosemia Infants with classic galactosemia usually present in the first few days after
birth and initiation of breast milk or cow's milk-based formula feedings. Typical symptoms
include jaundice, vomiting, hepatomegaly, failure to thrive, poor feeding, and susceptibility to
gram-negative infections; some develop lenticular cataracts. (See "Galactosemia: Clinical
features and diagnosis".)
Hereditary fructose intolerance Most cases of hereditary fructose intolerance present with
recurrent hypoglycemia and vomiting at the age of weaning, when fructose or sucrose (a
disaccharide that is hydrolyzed to glucose and fructose) typically is added to the infant diet.
However, some infants may present earlier because many commercial formulas and medications
contain sucrose. (See "Etiology of hypoglycemia in infants and children", section on 'Hereditary
fructose intolerance'.)
Older infants and children Gastroenteritis is by far the most common disorder presenting with
vomiting in infants, children, and adolescents (table 2). GERD, gastroparesis, mechanical
obstruction, anaphylaxis, Munchausen syndrome by proxy (factitious disorder by proxy),
intracranial masses, peptic ulcer disease, cyclic vomiting, and diabetic ketoacidosis also may be
diagnostic considerations. Adrenal crisis and anaphylaxis should be considered in children with
disproportionate hypotension and/or predisposing factors.

Gastroenteritis Gastroenteritis usually is viral in etiology, occurring in clusters, sudden in

onset, and quick to resolve. Bacterial causes may be associated with more prolonged and severe
illness. (See "Viral gastroenteritis in children: Epidemiology, clinical presentation, and
diagnosis" and "Clinical manifestations and diagnosis of rotavirus infection".)
Other infections Pharyngitis (particularly streptococcal pharyngitis) and urinary tract
infections frequently present with nausea and/or vomiting. (See "Approach to diagnosis of acute
infectious pharyngitis in children and adolescents", section on 'Group A Streptococcus' and
"Urinary tract infections in infants and children older than one month: Clinical features and
diagnosis", section on 'Clinical presentation'.)
Gastroparesis Gastroparesis is the condition of impaired emptying of gastric contents into the
duodenum in the absence of a mechanical obstruction; this may cause postprandial fullness and
nausea, and postprandial vomiting. In gastroparesis, the vomiting usually occurs many hours
after ingestion of food, a characteristic that differentiates this entity from gastroesophageal reflux
or rumination syndrome, in which the emesis occurs during or immediately after eating. (See
"Gastroparesis: Etiology, clinical manifestations, and diagnosis".)
The following conditions may cause gastroparesis:
Viral illness (postviral gastroparesis)
Surgery with vagus nerve damage (eg, fundoplication)
Use of drugs such as opioids or anticholinergics
Metabolic disturbances such as hypokalemia, acidosis, or hypothyroidism
Eosinophilic gastroenteropathy
Neuromuscular disorders such as cerebral palsy, diabetes mellitus, pseudo-obstruction, and
muscular dystrophy
Postviral gastroparesis is often found in children who have experienced an acute short viral
illness (often rotavirus gastroenteritis) and is associated with postprandial antral hypomotility. In
most cases, the symptoms resolve spontaneously within 6 to 24 months [8].
Intussusception Intussusception is the most common cause of intestinal obstruction in infants
between 6 and 36 months of age. Patients with intussusception typically develop the sudden
onset of intermittent, severe, crampy, progressive abdominal pain, accompanied by inconsolable
crying and drawing up of the legs toward the abdomen. The episodes become more frequent and
more severe over time. Vomiting may follow episodes of abdominal pain. Initially, emesis is
nonbilious, but it may become bilious as the obstruction progresses. A sausage-shaped abdominal
mass may be felt in the right side of the abdomen. As symptoms progress, increasing lethargy
develops, which can be mistaken for meningoencephalitis. In up to 70 percent of cases, the stool
contains gross or occult blood. (See "Intussusception in children".)

Intussusception also can occur in neonates and young infants. In infants, intussusception may
present as lethargy, with or without vomiting or rectal bleeding. In young infants, intussusception
is more often caused by a pathological lead point, such as Meckel diverticulum or a duplication
cyst.
Anaphylaxis Anaphylaxis, triggered by ingested items (typically foods or medications), tends
to present with prominent gastrointestinal symptoms, including nausea, crampy or colicky
abdominal pain, vomiting (sometimes large quantities of "stringy" mucus), and diarrhea. These
immediate (IgE-mediated) anaphylactic reactions are rapid in onset, typically beginning within
minutes to two hours from the time of ingestion.
During anaphylaxis, gastrointestinal symptoms usually are accompanied by various signs and
symptoms involving the skin and mucosa tissue, respiratory tract, and/or cardiovascular system.
These include pruritus, flushing, urticaria/angioedema, periorbital edema, conjunctival injection,
rhinorrhea, nasal congestion, cough, wheezing, dyspnea, change of voice quality, sense of
choking, tachycardia (or bradycardia less commonly), dizziness, hypotension, sense of
impending doom, and cardiovascular collapse. The gastrointestinal symptoms are rarely the sole
manifestations of a food-allergic reaction. In most cases, an allergic reaction to food can be
readily distinguished from other causes of vomiting by the presence of concurrent anaphylactic
symptoms and by the history. The diagnosis and treatment of anaphylaxis is reviewed separately.
(See "Anaphylaxis: Rapid recognition and treatment" and "Clinical manifestations of food
allergy: An overview" and "Food allergy in children: Prevalence, natural history, and monitoring
for resolution".)
Adrenal crisis Although it is uncommon, adrenal crisis should be considered in children of
any age, particularly if they have risk factors (such as known adrenal insufficiency or history of
glucocorticoid use), and/or present with disproportionate hypotension, hyponatremia, and/or
hyperkalemic acidosis. (See "Causes and clinical manifestations of primary adrenal insufficiency
in children", section on 'Adrenal crisis'.)
Intracranial hypertension Brain tumors and other intracranial masses can cause nausea,
vomiting, or both, by increasing the intracranial pressure (ICP) at the area postrema of the
medulla. (See "Elevated intracranial pressure (ICP) in children".)
Clinical characteristics suggesting increased ICP include emesis that is triggered by an abrupt
change in body position, especially upon awakening, with little or no accompanying nausea.
More importantly, neurogenic vomiting usually is associated with other neurologic symptoms
such as headache or focal neurologic deficit, although these signs and symptoms may be subtle.
(See "Clinical presentation and diagnosis of brain tumors".)
Idiopathic intracranial hypertension (pseudotumor cerebri) refers to increased ICP with normal
cerebrospinal fluid (CSF) content, normal neuroimaging, the absence of neurologic signs except
cranial nerve VI palsy, and no known cause. It is usually associated with headache, and
occasionally with nausea and vomiting. In the pediatric age range, it is most likely to affect
adolescent girls who are obese. (See "Idiopathic intracranial hypertension (pseudotumor cerebri):
Clinical features and diagnosis".)

Cyclic vomiting syndrome Cyclic vomiting syndrome is a disorder characterized by repeated

episodes of nausea and vomiting that last for hours to days separated by symptom-free periods of
variable length. This on-off pattern of emesis is quite distinct from most other causes of
vomiting. Intense vomiting and nausea are the cardinal symptoms and usually lead to significant
deficits of fluids and electrolytes. Cyclic vomiting has been most often described in school-aged
children, but may affect other age groups. The etiology is unknown, although many hypotheses
have been proposed. An association between cyclic vomiting syndrome and migraine headaches
has been most consistently described, suggesting that there may be a common pathophysiologic
process. (See "Cyclic vomiting syndrome".)
Migraine Migraine is characterized by periodic episodes of paroxysmal headache often
accompanied by nausea, vomiting, abdominal pain, and relief with sleep. The disorder occurs at
all ages, beginning before age 20 years in 50 percent of cases. The family history is positive in
most patients. Migraine usually can be distinguished from other causes of vomiting by the
periodic nature and associated characteristic headache with photophobia and phonophobia. (See
"Pathophysiology, clinical features, and diagnosis of migraine in children".)
Eosinophilic esophagitis or gastroenteritis Eosinophilic disease can affect multiple parts of the
upper gastrointestinal tract, together or separately. In eosinophilic esophagitis, boys compared
with girls are disproportionately affected 4:1. Toddlers tend to experience epigastric pain, nausea
and vomiting, and feeding aversion. Adolescents tend to have symptoms of dysphagia and may
present acutely to the emergency department with a food impaction [9]. In many cases, the
disorder appears to be mediated by a delayed, cell-mediated hypersensitivity to foods. Many but
not all patients have associated allergic disorders such as eczema and asthma. (See "Clinical
manifestations and diagnosis of eosinophilic esophagitis".)
Eosinophilic gastroenteritis can present at any age with abdominal pain, nausea, diarrhea,
malabsorption, hypoalbuminemia, and weight loss. In infants, it may present as outlet obstruction
with postprandial projectile vomiting. In adolescents and adults, it can also present with nausea
and vomiting, or may mimic irritable bowel syndrome. Symptoms vary depending on the layer
and site of involved gastrointestinal tract. Approximately one-half of patients have allergic
disease, such as defined food sensitivities, asthma, eczema, or rhinitis. (See "Eosinophilic
gastroenteritis".)
Munchausen syndrome by proxy Munchausen syndrome by proxy (also known as factitious
disorder by proxy, Meadow syndrome, and proxy factitia) consists of fabricating or inducing
illness in a child in order to get attention. The patient may have a history of frequent recurrent
illnesses without a clear etiology. As an example, ipecac poisoning can present with recurrent,
unexplained vomiting and repeated hospitalizations, and can be confirmed by urine toxicology
[10,11]. (See "Medical child abuse (Munchausen syndrome by proxy)".)
The diagnosis should be considered if the following features are present:
The reported history varies from what is observed or does not make sense.

The illness is unexplained, unusual, or prolonged, and does not respond to treatment as
expected.
The symptoms seem to originate only in the presence of the suspected perpetrator.
The problem resolves or improves when the child is separated from the suspected perpetrator.
The problem recurs when the suspected perpetrator is told that the child is improving or is soon
to be released from the hospital or treatment program.
Family members (eg, siblings) have unexplained symptoms, illness, or death.
The suspected perpetrator behaves in a manner that appears to be consistent with exaggeration,
fabrication, or induction of physical, psychological, or behavioral problems in the child.
The alleged perpetrator does not seem to be as worried by the child's illness as the health
professionals who are caring for the child.
Adolescents In addition to the disorders affecting children listed above (see 'Older infants and
children' above), some of the more common causes of nausea and vomiting in adolescents
include gastroenteritis, appendicitis, inflammatory bowel disease (IBD), pregnancy, and toxic
ingestions (table 2).
Functional dyspepsia Dyspepsia is defined by a persistent or recurrent pain or discomfort
localized to the upper abdomen; it is often associated with postprandial nausea, vomiting, and
early satiety. In most cases, dyspepsia appears to be functional in nature due to a disorder of
upper gastrointestinal sensation and motility [12]. Patients with functional dyspepsia often report
nausea, but persistent vomiting is uncommon. Dyspepsia may occasionally arise from an organic
disease such as peptic ulcer (with or without underlying Helicobacter pylori [H. pylori]
infection), food allergy, or Crohn disease. The approach to the adolescent patient with dyspeptic
symptoms, and a more detailed discussion of functional dyspepsia are given separately. (See
"Chronic abdominal pain in children and adolescents: Approach to the evaluation", section on
'Functional disorders' and "Approach to the adult with dyspepsia".)
Appendicitis Appendicitis presents most frequently in the second decade of life and is the
most common indication for emergent abdominal surgery in childhood. Early signs and
symptoms of appendicitis are often subtle, and may vary depending upon the location of the
appendix. An inflamed anterior or pelvic appendix produces marked symptoms in the right lower
quadrant, while a retrocecal appendix may not cause the same degree of local signs of peritonitis
because the inflammation is masked by the overlying bowel.
In many patients, initial features are nonspecific, including indigestion, flatulence, bowel
irregularity, and sometimes just a sense of feeling unwell. These symptoms usually are followed
by pain in the epigastrium or periumbilical region, which is visceral in character (ie, constant, not
very severe in intensity, and poorly localizable). The symptoms eventually localize to the right
lower quadrant once inflammation involves the overlying parietal peritoneum. Nausea and

vomiting, if they occur, follow the onset of pain. The diagnosis of appendicitis is less likely in
patients in whom nausea and emesis are the first signs of illness. (See "Acute appendicitis in
children: Clinical manifestations and diagnosis".)
Inflammatory bowel disease IBD (ulcerative colitis and Crohn disease) may present with
complaints of nausea, but frank vomiting is rarely a primary presenting symptom. The disease
should be considered if there are suggestive features in the history and clinical presentation,
especially growth failure, anemia, abdominal pain, perianal disease, bloody diarrhea, or arthritis.
(See "Clinical presentation and diagnosis of inflammatory bowel disease in infants, children, and
adolescents".)
Pregnancy Pediatricians should have a low threshold for suspecting pregnancy in adolescents.
Adolescents may or may not have considered the possibility of pregnancy or may present with
vague complaints with suspected pregnancy as her "hidden agenda." (See "Pregnancy in
adolescents", section on 'Diagnosis of pregnancy'.)
Bulimia or psychogenic vomiting Bulimia nervosa should be considered in a patient with
concerns about body weight and shape. Psychogenic vomiting is more likely in a patient with an
anxiety disorder, or may coincide with particularly stressful situations. (See "Eating disorders:
Overview of epidemiology, diagnosis, and course of illness" and "Somatization: Epidemiology,
pathogenesis, clinical features, medical evaluation, and diagnosis".)
Adolescent rumination syndrome Rumination syndrome, characterized by effortless
regurgitation and/or re-swallowing of food, has previously been recognized as a disorder of
emotionally-deprived infants. More recently, it was recognized as a problem of older children
and adolescents [13]. Some patient groups, such as adolescent girls, are at higher risk of
rumination syndrome. It has been suggested that this condition may be considered an early or
incomplete form of an eating disorder. The severity of adolescent rumination syndrome varies,
ranging from a benign disorder, amenable to behavioral therapies, to much more severe forms
associated with substantial weight loss and inability to attend school. (See "Eating disorders:
Overview of epidemiology, diagnosis, and course of illness", section on 'Rumination disorder'.)
The characteristic of this condition is the presence of regurgitation without nausea immediately
after eating. The symptoms disappear hours after eating once the regurgitated material becomes
acidic, and do not occur during sleep. The clinical characteristics and diagnosis of rumination
syndrome are discussed in more detail separately. (See "Gastroparesis: Etiology, clinical
manifestations, and diagnosis", section on 'Differential diagnosis'.)
TREATMENT Treatment should be directed toward the underlying etiology. Electrolyte
abnormalities, metabolic abnormalities, or nutritional deficiencies should be corrected.
Cognitive-behavioral interventions are useful for vomiting associated with functional dyspepsia,
adolescent rumination syndrome, and bulimia.
Antiemetics are useful for selected causes of persistent vomiting, to avoid electrolyte
abnormalities or nutritional sequelae. They typically are not recommended for vomiting of
unknown etiology, and are not appropriate for treatment of vomiting caused by anatomic

abnormalities or surgical abdomen; they are also contraindicated in infants. Selection of

antiemetics varies with the cause of the vomiting, as summarized in the table (table 8); more
details are available in the linked topic reviews:
Gastroenteritis. (See "Oral rehydration therapy", section on 'Vomiting' and "Viral gastroenteritis
in children: Prevention and treatment", section on 'Antiemetic agents'.)
Cyclic vomiting syndrome. (See "Cyclic vomiting syndrome", section on 'Treatment'.)
Motion sickness The first-line approach for preventing motion sickness is to avoid
environmental triggers, such as reading or viewing a screen while riding in a car. Drug therapy
for motion sickness depends upon inhibition of activity in the vestibular nuclei, where
labyrinthine and visual sensory cues are combined and synthesized. Drugs that reduce activity in
the vestibular nuclei include antihistamines and anticholinergics [2]. (See "Motion sickness",
section on 'Medication'.)
Gastroparesis The prokinetic agents erythromycin, metoclopramide, and domperidone have a
role in the management of chronic intestinal pseudo-obstruction and gastroparesis (including
post-viral gastroparesis) [8]. The US Food and Drug Administration (FDA) has issued a "boxed
warning" about the potential for tardive dyskinesia associated with chronic or high dose use of
metoclopramide. Hence, this drug should be used only after a careful discussion with the patient
and the caretakers about its possible risks and benefits. Drug selection and the potential adverse
effects of these drugs are discussed separately. (See "Chronic intestinal pseudo-obstruction",
section on 'Treatment' and "Treatment of gastroparesis", section on 'Prokinetics'.)
Postoperative nausea and vomiting During the last two decades, there have been considerable
advances in the development of antiemetics. These include the emergence of 5hydroxytryptamine 3 receptor (5-HT3) antagonists (ondansetron, granisetron), which have one
primary site of antagonism and have helped in the treatment of postoperative nausea and
vomiting, and chemotherapy-associated emesis [2,14].
Chemotherapy-induced nausea and vomiting Tremendous strides have been made in
development of antiemetics over the past two decades, especially 5-HT3 antagonists
(ondansetron) and neurokinin 1 (NK1) antagonists (aprepitant). Factors that increase the
incidence of vomiting include young age (toddler), female sex, agent emetogenicity (especially
cisplatin), and higher rate of administration. 5-HT3 antagonists are generally effective in the
acute phase the first 24 hours, whereas NK1 antagonists are more effective in the delayed phase
>24 hours.
Patients and families are increasingly turning to complementary and alternative medicine for a
variety of complaints, particularly if the symptom is chronic or does not have a clear diagnostic
explanation [15]. Applications of these techniques to the symptoms of nausea and vomiting have
not been well-studied, but there is some evidence for efficacy of some nutraceuticals, such as
ginger and other herbal compounds for functional dyspepsia and other motility disorders
[12,16,17]. Hypnotherapy is often helpful for treatment of anticipatory nausea and vomiting (eg,
prior to chemotherapy) [18], whereas studies of hypnotherapy for functional dyspepsia are less

conclusive [19-21]. The definitions and general approaches of other complementary and
alternative techniques are discussed separately. (See "Overview of complementary and
alternative medicine in pediatrics".)
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials,
"The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain
language, at the 5th to 6th grade reading level, and they answer the four or five key questions a
patient might have about a given condition. These articles are best for patients who want a
general overview and who prefer short, easy-to-read materials. Beyond the Basics patient
education pieces are longer, more sophisticated, and more detailed. These articles are written at
the 10th to 12th grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)
Basics topic (see "Patient information: Pyloric stenosis in babies (The Basics)")
Beyond the Basics topic (see "Patient information: Nausea and vomiting in infants and children
(Beyond the Basics)")
SUMMARY The symptoms of nausea and vomiting may be caused by a wide range of
conditions affecting several different organ systems, with vastly different health implications.
The immediate goal of the evaluation is to recognize serious conditions for which immediate
intervention is required, and then to identify a specific cause of the symptoms.
The causes of vomiting vary by age. Many of these disorders present in several age ranges, but
can be grouped into age ranges in which they present most frequently (table 2). (See 'Differential
diagnosis of vomiting by age group' above.)
In many cases, the cause of the nausea and vomiting can be determined from the history and
physical examination. The differential diagnosis is informed by the child's age, whether the
nausea and vomiting is acute, chronic, or episodic. Certain clinical features may offer diagnostic
clues that can further narrow the differential diagnosis (table 4). Laboratory testing should be
performed to screen for causes of the symptom, guided by the history and physical examination
(table 5). (See 'Evaluation' above.)
Concerning signs The history and physical examination provides important clues to
disorders requiring urgent intervention (table 3) (see 'Concerning signs' above and 'History'
above and 'Physical examination' above):
Prolonged vomiting (eg, >12 hours in a neonate; >24 hours in children younger than two years;
>48 hours in older children) suggests a cause that may require urgent intervention. In addition,
patients with prolonged vomiting are at risk for developing dehydration and electrolyte
abnormalities.

Symptoms and signs suggestive of intestinal obstruction include marked abdominal distension,
visible bowel loops, absent bowel sounds or increased high-pitched bowel sounds
("borborygmi"), severe abdominal pain, or vomitus that is bilious (green or yellow) or feculent
(with the odor of feces). Bilious vomiting is a particularly important warning sign of possible
intestinal obstruction in a neonate (eg, due to intestinal atresia or volvulus). (See 'Intestinal
obstruction' above.)
The sudden onset of intermittent, severe, crampy, progressive abdominal pain in an infant or
toddler suggests the possibility of intussusception, which is the most common cause of intestinal
obstruction in infants between 6 and 36 months of age. (See 'Intussusception' above.)
Headache, positional triggers for vomiting, lack of nausea, and/or vomiting on awakening
suggest the possibility of increased intracranial pressure. An adolescent female with early
morning vomiting also should be evaluated for pregnancy. (See 'Intracranial hypertension'
above.)
Altered consciousness, seizures, or focal neurologic abnormalities suggest the possibility of
toxic ingestion or central nervous system mass (all ages), inborn error of metabolism (primarily
infants and toddlers), or diabetic ketoacidosis (DKA, primarily children and adolescents). (See
'Intracranial hypertension' above and 'Inborn errors of metabolism' above.)
Recurrent episodes of vomiting and dehydration in an infant or young child suggest the
possibility of an inborn error of metabolism, particularly organic acidemias and urea cycle
disorders. Similar patterns are seen in cyclic vomiting syndrome, which is most common in
school-aged children. Migraine also may present with periodic vomiting, but can usually be
distinguished by the family history of migraine and associated headache. (See 'Inborn errors of
metabolism' above and 'Cyclic vomiting syndrome' above and 'Migraine' above.)
Hypotension disproportionate to the apparent illness and/or hyperkalemia suggests the
possibility of adrenal crisis. (See 'Adrenal crisis' above.)